Effects of recombination-deficient and repair-deficient loci on meiotic and mitotic chromosome behavior in Drosophila melanogaster.
The results of recent genetic and cytological studies on recombination-defective and repair-defective mutants of Drosophila melanogaster are summarized. These studies show that there is substantial overlap between the functions used in various aspects of DNA metabolism in Drosophila. Most loci first identified by either recombination-defective or mutagen-sensitive mutants have been shown also to function in nonmutagenized mitotic cells where their action is necessary to maintain the integrity of the genome: mutants at particular loci produce elevated frequencies of chromosome breakage, mitotic exchange, mutation, and/or chromosome loss. Genetic studies of meiotic recombination show that many of the loci identified by recombination-defective mutants restrict where along the chromosome arms exchange may occur. Recent EM studies suggest that the products of at least some of these loci are components of recombination nodules. Region-specific control of DNA metabolism is also indicated by the finding of nonrandom patterns of chromosome breakage in some mutagen-sensitive mutants. Recombination-defective mutants at two loci have been studied for their effects on sister chromatid exchanges (SCEs) and x-ray induced aberrations. Mutants at both loci are defective in steps necessary for the production of symmetrical chromatid interchanges but have little effect on SCEs.
D000818:Animals; D002869:Chromosome Aberrations; D002875:Chromosomes / Q000378:metabolism* / Q000528:radiation effects; D004260:DNA Repair; D004331:Drosophila melanogaster / Q000235:genetics* / Q000528:radiation effects; D008540:Meiosis; D008938:Mitosis; D011995:Recombination, Genetic; D012854:Sister Chromatid Exchange